Pancreas · 2012
Effects of c-Jun N-terminal kinase signaling pathway on severe acute pancreatitis-associated lung injury.
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Liu Mingdong, Shi Liangliang, Chen Min, Chen Suyu, Zou Xiaoping
Аннотация
OBJECTIVE: The objective of this study was to investigate the effects of the c-Jun N-terminal kinase (JNK) signaling pathway on rats' acute pancreatitis-associated lung injury (APALI).
METHODS: Seventy-two Sprague-Dawley rats were randomly divided into 3 groups, namely, the sham operation (SO) group, the severe acute pancreatitis (SAP) group, and the SP600125 group. The SAP model was established by injection of 5% sodium taurocholate into the pancreatic duct. The samples were taken at 3, 6, 12, and 24 hours. Serum amylase, pathologic lesions of the pancreas and lung tissues, wet-to-dry weight ratio of the lung, myeloperoxidase (MPO) activity of the lung, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), intercellular adhesion molecule 1 (ICAM-1), and p-JNK of lung tissues were detected.
RESULTS: The wet-to-dry weight ratio, MPO activity, and IL-1β, TNF-α, ICAM-1, and p-JNK levels in the SAP group significantly increased compared with those in the SO group. The scores of lung pathologic injury significantly increased, consistent with the APALI. The wet-to-dry weight ratio, MPO activity, IL-1β, TNF-α, ICAM-1, p-JNK expressions, and lung pathologic injury scores in the SP600125 group decreased compared with those in the SAP group. p-JNK was closely correlated with MPO activity, IL-1β, ICAM-1, and total scores of lung injury.
CONCLUSIONS: The JNK signaling pathway plays a critical role in APALI. On the other hand, application of a specific JNK inhibitor can contribute to alleviation of APALI.
METHODS: Seventy-two Sprague-Dawley rats were randomly divided into 3 groups, namely, the sham operation (SO) group, the severe acute pancreatitis (SAP) group, and the SP600125 group. The SAP model was established by injection of 5% sodium taurocholate into the pancreatic duct. The samples were taken at 3, 6, 12, and 24 hours. Serum amylase, pathologic lesions of the pancreas and lung tissues, wet-to-dry weight ratio of the lung, myeloperoxidase (MPO) activity of the lung, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), intercellular adhesion molecule 1 (ICAM-1), and p-JNK of lung tissues were detected.
RESULTS: The wet-to-dry weight ratio, MPO activity, and IL-1β, TNF-α, ICAM-1, and p-JNK levels in the SAP group significantly increased compared with those in the SO group. The scores of lung pathologic injury significantly increased, consistent with the APALI. The wet-to-dry weight ratio, MPO activity, IL-1β, TNF-α, ICAM-1, p-JNK expressions, and lung pathologic injury scores in the SP600125 group decreased compared with those in the SAP group. p-JNK was closely correlated with MPO activity, IL-1β, ICAM-1, and total scores of lung injury.
CONCLUSIONS: The JNK signaling pathway plays a critical role in APALI. On the other hand, application of a specific JNK inhibitor can contribute to alleviation of APALI.
Предметные рубрики MeSH
Acute DiseaseAmylasesAnimalsAnthracenesDisease Models, AnimalIntercellular Adhesion Molecule-1Interleukin-1JNK Mitogen-Activated Protein KinasesLungLung InjuryMalePancreasPancreatitisPeroxidasePhosphorylationProtein Kinase InhibitorsRatsRats, Sprague-DawleySignal TransductionTaurocholic AcidTime FactorsTumor Necrosis Factor-alpha